Is that percentage by weight, percentage by dry weight, percentage by calories, or something else?
And no matter which I interpret it as, all those diets are "protein and fat based" by Standard American Diet standards. Seeds and nuts are very high in fat.
> Bread was the staple food for most of that period.
No, not really. The refined white flour we eat today basically didn't exist until very recently.
Their bread wasn't like our bread. It was coarsely-ground and made of bran, barley and rye. Compared to what we eat today, it had much higher fiber content and more fat. It would have been much harder for our ancestors to mainline pure carbohydrates by eating bread like we do.
Carbs in themselves aren't so bad, but the problem is that your body won't ever be sated by eating carbohydrates. (Kids around Halloween will attest.) Eating pure carbs is a very bad idea.
The problem is carbs give you short term energy. It's great and healthy if you're doing manual labor, playing sports, lifting weights, etc. or otherwise burning that caloric intake.
If you're watching TV and eating carbs your energy boost is wasted and can get stored as fat.
And sugar as far as far as I'm aware is never healthy but can have less of a health impact in very small doses.
Yeah, I begin to wonder if we need to be a little more specific when talking about this, e.g. not just "carbs" but "simple carbs" and "complex carbs", or "refined" & "unrefined". We've dealt with this once before with saturated & unsaturated fats, vs trans fats.
Carbs are carbs. The biggest problem is that you won't feel full or know when to stop if you're eating just carbs. You need fats or fibers to stop eating, hence "unrefined".
Also physical activity for most people took a nosedive in the past decades. Work has mostly shifted to static jobs and that shifts the balance of any diet.
Carbohydrates used to come from fruits (with fiber), vegetables (in small amounts & with fiber), and starchy vegetables (starches are complex & slow to digest). Today, carbohydrates are consumed in simpler forms and refined to be more concentrated.
In the former case, they digest slowly. In the latter case, they digest quickly. The practical implications of this are immediately obvious if you have ever heard of glycemic index and glycemic load, but in short, fast digestion & large quantities results in a big spike in blood sugar which is hard on your body & leads to diabetes.
Also important is that the original forms of carbohydrates came with all kinds of other nutrients. A sweet potato includes vitamin A, vitamin C, manganese, copper, pantothenic acid, vitamin B6, potassium, niacin, vitamin B1, vitamin B2 and phosphorus. Sugar on the other hand is the quintessential "empty calorie", carrying no vitamins, minerals, only calories.
For one, the amount of refined sugar in our diet exploded recently.
More generally, even if the molecular building blocks didn't change, the way food is prepared industrially and marketed makes us more likely to eat too much of it.
A lot of our modern economy seems to be relying on human predisposition to addictions. Think sugar / carbs, alcohol, tobacco, certain games, news and social media and their recommendation engines. All exploiting similar neural pathways.
In the country I live in, white flour must legally be mixed with iron. In natural foods, iron is bounds to proteins like hemoglobin or ferritin. Legally mandated iron is just "iron", which means whatever's cheapest, i.e. metallic iron powder. This is known to be poorly absorbed:
So what happens to the non-absorbed portion? I have read speculation that it could affect intestinal bacteria. Intestinal bacteria are poorly understood, but widely believed to affect human health. What happens when you start feeding them evolutionarily novel nutrients? I'm not claiming that it has any measurable effect, good or bad, but from a precautionary principle viewpoint it seems to me a bad idea.
Government dietary recommendations became politicized in 1980, and increasingly separated from both nutrition science and comprehensibility to the public with each 5-year revision. In 1967, the bacterium used to produce the enzyme that turns corn syrup into high-fructose corn syrup was perfected, and HFCS became available in industry. In 1983, it was confirmed as GRAS status, and started replacing sucrose sugar in foods. The food-industry had already been replacing fats with sugars as a result of popularized science suggesting that higher-fat diets were a causative factor for heart disease.
Purchasing power for below-median wage-earners has stagnated since the 1970s. Lower income levels correlate with higher obesity.
Climate-controlled buildings are now the norm. More efficient heaters and coolers make it cheaper to be in a 20 degree C environment year round. Clement climate correlates geographically with higher obesity.
Canine Distemper Virus has been shown (Lyons, 1982) to cause permanently-elevated levels of obesity in mice. Since then, other infectious diseases have been found to promote obesity in animals: RAV-7, Borna, Scrapie, SMAM-1, Ad-36, Ad-5, Ad-37. Gut parasites produced symptoms similar to metabolic syndrome in dragonflies. Obese humans have been found to have a 3 times higher incidence of evidence of past infection by adenovirus Ad-36 than the non-obese (30% vs. 11%). If twin studies, where one twin had been infected by Ad-36, and the other not, the exposed twin was fatter. Across all studies, evidence of past infection by Ad-36 always correlated with a fatter subject, with causative significance. It even works with viruses originating in nonhuman animals, that do not otherwise cause visible symptoms. A sick bird could make you fat, without ever making you sneeze.
Analyses of digestive tract microbiotic factors have discovered causative significance for obesity in some factors. Experimental fecal transplants have resulted in changes in the recipient's weight and body composition.
Studies of epigenetic DNA methylation, sibling genetics, and maternal weight suggest that children of obese mothers may have greater predisposition to obesity, creating an intergenerational feedback loop. Fat mothers make fat daughters make fat granddaughters. This could be experimentally verified by cloning/twinning a female animal embryo, applying different environmental factors to produce breeding animals of different obesity levels, and implanting each with a second set of clone embryos. The second set of clones would then be kept under identical environmental conditions. Unfortunately, cloning processes themselves introduce epigenetic regulations and deregulations that ultimately result in obesity. Cloned mice get fatter when they get older.
It seems as though older mothers bear children that grow fatter as adults. Children of moms over 30 have higher body fat percentages than children of moms under 25, by about 2.7 percentage points. Both low-birthweight and high-birthweight babies correlate to greater adult obesity, and older mothers are less likely to have middle-birthweight babies.
Sleep deprivation correlates with higher obesity.
In short:
change in foods composition \\\
wage stagnation \\\
literal adenovirus epidemics \\\
change in gut microbiota \\\ OBESITY
intergenerational epigenetics /// (complex cause)
delay in child-rearing ages ///
chronic sleep deprivation ///
other factors??? ///
- Poverty can't be causal here, since it doesn't match either the timing nor the geography of the epidemics.
- Intergenerational epigenetics is a secondary factor, but it can't be causative in the first generation.
- While the adenovirus study is interesting I'd be surprised its spread mapped with the time/space patterns of the obesity epidemics worldwide.
I mention geographical spread because the epidemics seems to spread along with industrialization, e.g. urban China is affected, while rural China isn't (yet?). The spread of the epidemics seems to map well with the spread of Western junk food.
The following parameters could somehow make sense if Japanese folks weren't so lean
- delay in child rearing (where the effect size is minor)
- chronic sleep deprivation (and wow, 1/3 US adults sleeps less than 6 hours per night whereas 1/3 gets more than 8 hours).
- Microbiota is interesting, but known to be influenced by diet. So a problematic microbiota could be a maladaptative change consecutive to a bad diet, that perpetuates the issue.
These factors also apply to Japan, which has resisted the junk food onslaught for cultural reasons. Japan has ~3% of obese folks, and that was the case before they started aggressively monitoring belly fat in middle aged folks. Japanese folks who migrate to the US and adopt the local diet grow fat, so the difference isn't genetic.
————
This leaves us with food composition and marketing as the main causal factors.
- Why can't poverty be causal? An essential part of food composition and marketing is price. As your disposable income decreases, the composition of items on the McDonald's value menu becomes more relevant to you, and the quality of the produce at Whole Foods markedly less so.
- Intergenerational epigenetic influence means that factors that are no longer overtly visible may have a lasting effect. If, for example, leaded gasoline exhaust fumes made grandma fat, that contributory cause could then invisibly propagate to a later generation via epigenetic regulation attached to gametes and occurring in utero.
- In 2011, someone suggested that Ad-26 and Ad-35 be used in an Ebola vaccine, to work around preexisting Ad-5 immunity in targeted populations. The anti-vaxxer nonsense notwithstanding, the hypothesis that an unknown obesity vector has been spread via routine vaccination, without any other adverse symptoms or side effects, has not yet been tested. Better fat than dead, though.
Several hypotheses regarding decrease in dietary quality have been tested, and found to be unsupported by evidence. The corn lobby has quite a vested interest in proving that HFCS is not significantly different from cane sugar sucrose in prepared foods, so you can find a lot of very narrow studies comparing HFCS to sucrose that all conclude they are the same dietarily, without going anywhere near price, or politics, or comparisons with the fats that both sucrose and HFCS have been replacing over the years. I foresee future studies declaring (cheap) palm oil to be dietarily equivalent to other (more expensive) oils, without ever noting the impact of prices on recipes and diets. Broader studies likely have a harder time getting funding.
Microbiota are also influenced by location--even temporary changes in location. Montezuma's Revenge and Delhi Belly and trail trots can all cause rapid change in one's gut constitution.
Observing Japanese who migrate to the US and preserve their previous diet could be elucidative. If they don't change anything about their lives other than their location, would they grow fatter?
Because most poor people around the world are not fat and have never been until recently. In the countries affected by the obesity epidemics, it may be causal, but it doesn't explain why obesity struck somewhere and not elsewhere.
> - Intergenerational epigenetic influence means that factors that are no longer overtly visible may have a lasting effect.
Agreed 100%, it has an impact in the long run, but as a secondary factor, not as a trigger.
> - vaccines
I don't understand the point you're tying to make (beside "fuck anti-vaxxers", and I couldn't agree more). Specifically, I don't understand the link between these specific anti-Ebola vaccines and the possibility that vaccines could cause obesity.
> - HFCS...
A high fructose diet causes non-alcoholic fatty liver disease (a close cousin of metabolic syndrome), and that is well established. In general I have little trust studies that are privately funded. Too much room for bias.
IIRC the Japanese who migrate and keep their traditional diet don't grow fat. This is purely out of memory though, from something I read or heard a long time ago, and I could be wrong.
In vaccines, viruses that are related to the target virus that present similar external structures may be used to train the immune system to target those structures. Immunity to the lesser virus confers immunity to the dangerous one. The specific suggestion was to change the viruses used in the Ebola vaccine, because too many people already had exposure and immunity to Ad-5. This implies that Ad-5 had been used in an earlier iteration of the vaccine. And Ad-5 is one of the adenoviruses that cause obesity.
Cowpox conferred immunity to smallpox--the similarity that led to the invention of vaccination in the first place.
It might be possible that some routine vaccination employs a virus that has always been considered completely harmless, with no visible symptoms beyond a little soreness and nasal sniffle, and that virus actually causes epigenetic changes that impact appetite and satiety, just like Ad-36, Ad-37, and Ad-5. There are about 50 known human adenoviruses, and less than 10 are believed to cause additional obesity. There are also viruses that are mainly pathogenic in other species, which cause no obvious symptoms whatsoever in humans--and in other species that are not the main host species--other than an increase in body fat. There are a lot of viruses out there. Only a small fraction have been studied extensively. Few would care to fund a test for antibodies to a virus that no one is afraid of, and that's what is needed to establish a correlation between exposure and obesity. The only reason adenoviruses were studied for this at all is because the avian virus that caused chickens to die fatter was denied an import license, and the researcher had to find something else that was already endemic.
Sometimes, a virus can be added as an adjuvant. It doesn't even have a direct impact on the targeted dangerous virus, it just makes the vaccine more effective by stirring up the immune system a little.
So it is entirely possible that vaccines that use live viruses that are traditionally considered harmless have never even tried to evaluate whether those viruses have impact on weight gain 10 to 20 years later. Those kids of anti-vaxxers that somehow survive to middle age might just end up with a lower average BMI than their vaccinated peers. It might be the only way we'd ever know. Usually, people who are not vaccinated live in a completely different culture, that would confound all the variables. An American anti-vaxxer living the same lifestyle (aside from the addled parents) as an immunized American would be a more apt comparison. The only other way to test would be to change the composition of the vaccine (an act that has an ethical impact) and wait a few decades to weigh people and caliper their back fat.
Hunter gathers ate whatever they could get, so varied a lot from place to place. As I understand it the Hadza's main source of calories is from tubers, so lots of carbs, just lots of fibre too.